FoxP3⁺ regulatory T cells inhibit ILC2 dependent AHR

2018-01-01Asthma is a heterogeneous disease of the lung airways. Innate Lymphoid Cells (ILC2s) have widely been accepted to potentiate allergic disease and asthma through their activation and production of Th2 cytokines as well as their cross-talk with Th2 cells. Pulmonary ILC2s are widely recognized after influenza infection, exposure to allergen or tissue damage to induce airway hyper-reactivity (AHR), a paramount feature of asthma in the absence of adaptive immunity. Recently, ILC2s have been proven to enhance Th2 initiation, proliferation and cytokine production leading to allergic lung inflammation. These allergic responses are modulated physiologically by Treg cells, who maintain tolerance to innocuous substances and limit incorrect or excessive immune responses. Several studies suggest that Treg cells are intimately involved in asthma tolerance solely through the direct inhibition of Th2 cells. However, currently the role of Treg cells in the control and modification of ILC2 cells has not been addressed. In the present study, we examined the suppressive effects of regulatory T cells on ILC2s. Exploring these Treg suppressive pathways may potentially lead to the design of methods controlling ILC2 and asthma